19 results on '"Davidoff, Olena"'
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2. Kidney epithelial targeted mitochondrial transcription factor A deficiency results in progressive mitochondrial depletion associated with severe cystic disease
3. Prolyl-4-hydroxylase 2 and 3 coregulate murine erythropoietin in brain pericytes
4. Distinct subpopulations of FOXD1 stroma-derived cells regulate renal erythropoietin
5. Renal epithelium regulates erythropoiesis via HIF-dependent suppression of erythropoietin
6. EPO synthesis induced by HIF‐PHD inhibition is dependent on myofibroblast transdifferentiation and colocalizes with non‐injured nephron segments in murine kidney fibrosis
7. Inhibition of hypoxia-inducible factor-prolyl hydroxylation protects from cyclophosphamide-induced bladder injury and urinary dysfunction
8. Endothelial HIF-2 mediates protection and recovery from ischemic kidney injury
9. Hepatic HIF-2 regulates erythropoietic responses to hypoxia in renal anemia
10. Hypoxia-inducible factor regulates hepcidin via erythropoietin-induced erythropoiesis
11. Inactivation of HIF-prolyl 4-hydroxylases 1, 2 and 3 in NG2-expressing cells induces HIF2-mediated neurovascular expansion independent of erythropoietin
12. Inhibition of hypoxia-inducible factor-prolyl hydroxylation protects from cyclophosphamide-induced bladder injury and urinary dysfunction.
13. Inactivation of HIF‐prolyl 4‐hydroxylases 1, 2 and 3 in NG2‐expressing cells induces HIF2‐mediated neurovascular expansion independent of erythropoietin
14. The role of hepatic EPO in non-uremic renal anemia
15. Inactivation of HIF‐prolyl 4‐hydroxylases 1, 2 and 3 in NG2‐expressing cells induces HIF2‐mediated neurovascular expansion independent of erythropoietin.
16. Hypoxia-inducible factor prolyl-4-hydroxylation in FOXD1 lineage cells is essential for normal kidney development
17. Hypoxia-inducible factor regulates hepcidin via erythropoietin-induced erythropoiesis.
18. Distinct subpopulations of FOXD1 stroma-derived cells regulate renal erythropoietin.
19. Disruption of mitochondrial electron transport impairs urinary concentration via AMPK-dependent suppression of aquaporin-2.
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